Exercise training improves functional capacity in patients with heart failure. This has been explained, in part, due to improvement in endothelial function leading to increased perfusion of the exercising skeletal muscles. Local oxidative stress is known to impair endothelial function. In this issue of Circulation, Linke et al evaluate whether exercise training reduces oxidative stress in patients with heart failure. In this controlled trial, 6 months of moderate-intensity exercise augmented the activity of the radical scavenger enzymes superoxide dismutase, catalase, and glutathione peroxidase and decreased oxidative stress, as measured by nitrotyrosine formation, in the skeletal muscle. In their elegant study, these authors have further elucidated important mechanisms by which exercise training is beneficial to patients with heart failure. See p 1763.

PROGNOSTIC VALUE OF AMBULATORY AND HOME BLOOD PRESSURES COMPARED WITH OFFICE BLOOD PRESSURE IN THE GENERAL POPULATION: FOLLOW-UP RESULTS FROM THE PRESSIONI ARTERIOSE MONITORATE E LORO ASSOCIAZIONI (PAMELA) STUDY, by Sega et al.

Ambulatory and home blood pressure measurement is often promoted as having greater prognostic importance than office-based measurement. In a general population, however, whether it is worth the extra effort to obtain ambulatory or home blood pressure measurement remains controversial. Investigators from Italy, using data from the PAMELA study, were able to compare the prognostic importance of ambulatory, home, and office blood pressure measurements for the risk of mortality in 2051 subjects who were followed up for an average of 131 months. The study provides evidence about whether a more comprehensive blood pressure measurement strategy applied to the general population would yield greater information about patients’ risk levels. See p 1777.

Among patients presenting with venous thrombosis, the presence of factor V Leiden has proven to be quite prevalent. Despite this well-known association, it is not clear if the presence of this genetic mutation has a material impact on arterial thrombosis. This question has been addressed in this issue via a mouse model. The investigators found that factor V Leiden was associated with a predilection to thrombosis. More importantly, however, this study was also able to address the source of factor V Leiden using a strategy of bone marrow transplantation. These data enhance our understanding of how factor V Leiden produces a predisposition to vascular thrombosis and the source(s) of factor V Leiden that cause this defect. See p 1822.